ObjectiveTo explore the relationship between acne vulgaris and gut microbiota. MethodsA total of 29 clinical cases diagnosed with moderate-to-severe acne vulgaris and 26 healthy individuals as control subjects were recruited. Fecal specimens were collected from all participants， and further analysis of gut microbial communities was performed by leveraging high-throughput sequencing techniques that target the hypervariable regions of 16S rRNA genes. ResultsAssociations between acne vulgaris and alterations in gut microbiota were identified. At the phylum level， the relative abundance of Bacteroidota exhibited a statistically significant elevation in the acne vulgaris cohort when compared with the healthy control group （P<0.01）， while Cyanobacteria was significantly lower in the acne group （P<0.01）. At the genus level， the top five different bacterial taxa in both groups were Bacteroides， Escherichia⁃Shigella， Klebsiella， Roseburia， and Parabacteroides. Among them， Bacteroides， Roseburia， and Parabacteroides were more abundant in acne patients. Linear discriminant analysis identified five biomarkers all belonging to the Bacteroidota phylum in the acne and control groups. These biomarkers belong to the phylum Bacteroidetes. ConclusionThere are significant differences in the composition of intestinal microbiota between acne patients and healthy people. Changes in the richness of specific bacterial genera may become new targets for the diagnosis and treatment of acne.

Non-alcoholic fatty liver disease （NAFLD） is one of the most prevalent forms of liver diseases globally. Its progression can lead to cirrhosis and end-stage liver disease， and there is currently a lack of effective pharmacological treatments. Adenosine monophosphate-activated protein kinase （AMPK）， as a regulatory hub for maintaining cellular energy homeostasis， can coordinate key cellular processes such as adipogenesis， glucose metabolism， and mitochondrial functions. Its activation exerts metabolic regulatory effects through pathways including inhibiting lipogenesis， enhancing mitochondrial β-oxidation， regulating inflammation and oxidative stress， and promoting autophagy. Accordingly， AMPK emerges as a potential target for the prevention and treatment of NAFLD. Traditional Chinese Medicine （TCM）， with low toxicity， high accessibility， and multi-component， multi-target synergistic effects， has demonstrated unique value in NAFLD treatment， particularly showing notable advantages in regulating the AMPK signaling pathway. Sichuan is known as the treasure house of TCM， and the active components of its authentic medicinal materials such as Coptidis Rhizoma not only reflect regional characteristics in AMPK signaling regulation but also form a multi-level metabolic regulatory network through crosstalk with pathways such as sirtuin 1 （SIRT1） and peroxisome proliferator-activated receptor α （PPARα）. They can achieve specific regulation by directly activating AMPK and modulating upstream and downstream targets， exerting prominent effects in ameliorating hepatic steatosis and inflammation. This study systematically reviews the research findings on TCM for the prevention and treatment of NAFLD over the past five years， elaborating the mechanisms by which TCM treats NAFLD through regulating the AMPK signaling pathway. It aims to provide new perspectives and references for clinical diagnosis and treatment， basic research， and drug development.

ObjectiveTo screen for and validate key differentially expressed proteins in serum of patients with metabolic dysfunction‑associated fatty liver disease （MAFLD）， and to provide a basis for identifying diagnostic biomarkers and developing intervention strategies for this disease. MethodsA total of 20 patients who were diagnosed with MAFLD in the third affiliated hospital of Chengdu University of Traditional Chinese Medicine from December 2024 to January 2025 were enrolled as MAFLD group， and 20 healthy controls were enrolled as HC group. Demographic data and serum biochemical parameters were collected from both groups. Data-independent acquisition （DIA） quantitative proteomics was used to measure the relative expression levels of serum proteins， and related methods were used to obtain significantly differentially expressed proteins， including the gene ontology functional enrichment analysis， the Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis， protein-protein interaction （PPI） network， Hub node interaction， and weighted gene co-expression network analysis （WGCNA）. Rats were given a high-fat diet to establish a model of MAFLD， and randomly assigned to the control group and model group. Serum biochemical parameters and inflammatory factors were measured， liver histopathological changes were observed， and the protein expression levels of MER proto-oncogene tyrosine kinase （MERTK） and matrix metalloproteinase-9 （MMP-9） in liver tissue were verified. The independent-samples t test was used for comparison of normally distributed continuous data between groups， while the Mann-Whitney U test was used for comparison of non-normally distributed continuous data or data with heterogeneity of variance between groups； the chi-square test or the Fisher’s exact test was used for comparison of categorical data between groups. ResultsCompared with the HC group， the MAFLD group had significant increases in the serum levels of aspartate aminotransferase （t=-7.348， P<0.05）， alanine aminotransferase （Z=5.088， P<0.05）， alkaline phosphatase （t=-3.943， P<0.05）， triglyceride （Z=2.070， P<0.05）， and high-density lipoprotein cholesterol （t=3.867， P<0.05）. A total of 3 559 proteins were identified by DIA serum proteomics， among which 160 differentially expressed proteins were mainly enriched in pathways including metabolic disorders， immune inflammatory response， and extracellular matrix remodeling. The PPI network and the Hub node analysis showed that serpin family E member 1， MMP-9， and intercellular cell adhesion molecule-1 were core regulatory proteins. WGCNA showed that the MEyellow module was significantly positively correlated with MAFLD phenotype （cor=0.55， P<0.001）， which was functionally enriched in the efferocytosis pathway. MERTK （P<0.001） and MMP-9 （P<0.001） showed the most significant differential expression in this module. A rat model of MAFLD was successfully established using a high-fat diet， and compared with the control group， the model group had enlarged， yellowish， and greasy liver and disordered structure of hepatic lobules， hepatocyte fatty degeneration， and inflammatory cell infiltration based on HE staining， as well as massive lipid droplet deposition based on oil red O staining， while no obvious fibrous cords were observed in Masson staining. Compared with the control group， the model group had significant increases in the serum levels of aspartate aminotransferase （t=-5.148， P<0.05）， alanine aminotransferase （t=-5.663， P<0.05）， total bilirubin （t=-13.061， P<0.05）， triglyceride （Z=-2.722， P<0.05）， total cholesterol （t=3.588， P<0.05）， and tumor necrosis factor-α （t=-16.741， P<0.05）， as well as significant increases in the protein expression levels of MERTK （t=-11.448， P<0.001） and MMP-9 （t=-10.875， P<0.001） in liver tissue. ConclusionMMP-9 and MERTK are abnormally expressed in MAFLD and may be used as potential diagnostic biomarkers for this disease.

Tumor drug resistance is an important problem in the failure of chemotherapy and targeted drug therapy, which is a complex process involving chromatin remodeling. SWI/SNF is one of the most studied ATP-dependent chromatin remodeling complexes in tumorigenesis, which plays an important role in the coordination of chromatin structural stability, gene expression, and post-translation modification. However, its mechanism in tumor drug resistance has not been systematically combed. SWI/SNF can be divided into 3 types according to its subunit composition: BAF, PBAF, and ncBAF. These 3 subtypes all contain two mutually exclusive ATPase catalytic subunits (SMARCA2 or SMARCA4), core subunits (SMARCC1 and SMARCD1), and regulatory subunits (ARID1A, PBRM1, and ACTB, etc.), which can control gene expression by regulating chromatin structure. The change of SWI/SNF complex subunits is one of the important factors of tumor drug resistance and progress. SMARCA4 and ARID1A are the most widely studied subunits in tumor drug resistance. Low expression of SMARCA4 can lead to the deletion of the transcription inhibitor of the BCL2L1 gene in mantle cell lymphoma, which will result in transcription up-regulation and significant resistance to the combination therapy of ibrutinib and venetoclax. Low expression of SMARCA4 and high expression of SMARCA2 can activate the FGFR1-pERK1/2 signaling pathway in ovarian high-grade serous carcinoma cells, which induces the overexpression of anti-apoptosis gene BCL2 and results in carboplatin resistance. SMARCA4 deletion can up-regulate epithelial-mesenchymal transition (EMT) by activating YAP1 gene expression in triple-negative breast cancer. It can also reduce the expression of Ca²⁺ channel IP3R3 in ovarian and lung cancer, resulting in the transfer of Ca²⁺ needed to induce apoptosis from endoplasmic reticulum to mitochondria damage. Thus, these two tumors are resistant to cisplatin. It has been found that verteporfin can overcome the drug resistance induced by SMARCA4 deletion. However, this inhibitor has not been applied in clinical practice. Therefore, it is a promising research direction to develop SWI/SNF ATPase targeted drugs with high oral bioavailability to treat patients with tumor resistance induced by low expression or deletion of SMARCA4. ARID1A deletion can activate the expression of ANXA1 protein in HER2+ breast cancer cells or down-regulate the expression of progesterone receptor B protein in endometrial cancer cells. The drug resistance of these two tumor cells to trastuzumab or progesterone is induced by activating AKT pathway. ARID1A deletion in ovarian cancer can increase the expression of MRP2 protein and make it resistant to carboplatin and paclitaxel. ARID1A deletion also can up-regulate the phosphorylation levels of EGFR, ErbB2, and RAF1 oncogene proteins.The ErbB and VEGF pathway are activated and EMT is increased. As a result, lung adenocarcinoma is resistant to epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs). Although great progress has been made in the research on the mechanism of SWI/SNF complex inducing tumor drug resistance, most of the research is still at the protein level. It is necessary to comprehensively and deeply explore the detailed mechanism of drug resistance from gene, transcription, protein, and metabolite levels by using multi-omics techniques, which can provide sufficient theoretical basis for the diagnosis and treatment of poor tumor prognosis caused by mutation or abnormal expression of SWI/SNF subunits in clinical practice.

Objective To explore the effect of PCSK9 inhibitor combined with atorvastatin on carotid atherosclerosis and its anti-inflammatory effect in patients with hypertension complicated with type 2 diabetes mellitus.Methods A total of 100 patients with hypertension complicated with type 2 diabetes mellitus who were treated in Nanchang Third Hospital from October 2022 to August 2023 were selected as the research subjects.They were divided into the control group and the study group by the random number table method,with 50 cases in each group.Both groups of patients received conventional antihypertensive,hypoglycemic,and antiplatelet therapy.The control group took 20 mg of atorvastatin calcium tablets orally,once a night.On the basis of the control group,the study group was additionally given 150 mg of evolocumab injection(a PCSK9 inhibitor)by subcutaneous injection,once every two weeks.Both groups of patients were followed up for 24 weeks.The levels of blood lipids,blood glucose,inflammatory cytokines,carotid intima-media thickness(IMT),atherosclerotic plaque score and adverse reactions of the patients in the two groups before and after treatment were detected and compared.Results The levels of TC,TG and LDL-C in the study group after treatment were lower than those before treatment and those in the control group at the same period,and the differences were statistically significant(P＜0.05).The levels of IL-1,IL-6,TNF-α,hs-CRP,as well as the ca-rotid IMT and atherosclerotic plaque score in the study group after treatment were lower than those before treatment and those in the control group at the same period,and the differences were statistically significant(P＜O.05).During the treatment period,there was no significant difference in the occurrence of adverse reac-tions between the two groups(P＞0.05).Conclusion The combination of PCSK9 inhibitor and atorvastatin can effectively regulate the blood lipid levels of patients with hypertension complicated and type 2 diabetes mellitus,alleviate the inflammatory response,and improve the degree of carotid atherosclerosis in these pa-tients.

The key to the growth and metastasis of pancreatic ductal adenocarcinoma(PDAC)is its complex stromal microenvironment and significant cellular and spatial heterogeneity.It can utilize the interac-tion between cellular and non cellular components in the microenvironment to induce immune escape and drug resistance,thereby reducing patient survival rates.In recent years,relevant studies have revealed the presence of non cellular components in the tumor microenvironment-matrix metalloproteinases(MMP),which can par-ticipate in inflammatory responses and cancer development by hydrolyzing the extracellular matrix.This arti-cle reviews the role of several MMP in the progression of pancreatic cancer,which have been confirmed by pre-vious studies.At the same time,MMP that may be associated with pancreatic cancer,but whose specific mech-anism has not yet been clarified are discussed in depth,providing a basic theoretical basis for further research on MMP as therapeutic targets for pancreatic cancer.

Objective To explore the relationship the changes of Doppler ultrasound parameters before and after thrombolytic therapy in the patients with acute lower extremity deep venous thrombosis and the prognosis.Methods A total of 100 patients with acute lower extremity deep venous thrombosis from Decem-ber 2022 to December 2024 were enrolled,given the thrombolytic therapy and received Doppler ultrasound ex-amination before and after treatment.The sonographic manifestations of the affected side detected by color Doppler ultrasound before treatment were statistically analyzed,and the changes of Doppler ultrasound param-eters of the affected side[end-diastolic velocity(EDV),peak systolic velocity(PSV),vascular resistance index(RI),vascular diameter at the lesion site]were compared between before and after treatment.According to whether pulmonary embolism occurred after thrombolysis,the patients were divided into the embolization group(n=29)and non-embolization group(m=71).The Doppler ultrasound parameters of the affected side before treatment were compared between the two groups.The binary logistic equation was adopted to analyze the related influencing factors of pulmonary embolism occurrence in the patients.The receiver operating char-acteristic(ROC)curve was used to analyze the predictive value of ultrasound parameters on pulmonary em-bolism.Results After thrombolytic therapy for the affected limb with acute lower extremity deep venous thrombosis,EDV,PSV and vascular diameter at the lesion site were decreased significantly,RI was increased significantly(P＜0.05).Before treatment,EDV.PSV,vascular diameter and the proportion of thrombus grade Ⅳ at the lesion site in the embolization group were significantly higher than those in the non-emboliza-tion group,the RI was significantly lower than that in the non-embolization group(P＜0.05).EDV,PSV,RI and the vascular diameter at the lesion site all were related to the occurrence of pulmonary embolism(P＜0.05).The areas under the curves(AUC)of SEDV,PSV,RI and vascular diameter at the lesion site in predic-ting the pulmonary embolism occurrence in the patients with acute lower extremity deep venous thrombosis were 0.690,0.717,0.649 and 0.662 respectively.The AUC of the 4-items combination in diagnosing the poor prognosis of the patients was 0.829,and the combined diagnostic value was higher.Conclusion EDV,PSV,vascular diameter and RI could predict the risk of pulmonary embolism occurrence after thrombolytic therapy in the patients with acute lower extremity deep venous thrombosis.

The traditional detection methods for monitoring the biomass,protein,chlorophyll content and other key indicators in the growth of chlorella have some problems,including complicated operation,slow detection speed and difficult large-scale application.In this study,a fast and efficient monitoring method for the key indicators in the growth of chlorella was established using near infrared spectroscopy and chemometrics.Near-infrared spectroscopy was used to collect near-infrared spectra of chlorella algal fluid at different growth stages,and standard methods were used to detect the biomass,protein and chlorophyll contents of corresponding samples.A quantitative analysis model was established based on partial least squares regression(PLSR).To improve the prediction ability of the model,multiplicative scatter correction(MSC)was used to reduce the interference of scattering on the raw spectrum(RS),standard normal variate(SNV)was used to normalize the original spectral data to eliminate differences between samples,continuous wavelet transform(CWT)was used to obtain the key features of spectral data,the first derivative(1st)was used to enhance the differentiation of the original spectral features,and monte carlo-uninformative variable elimination(MC-UVE)and randomization test(RT)were used to screen the valid variables in the wavelength.By evaluating the prediction ability of different models,the quantitative analysis models of chlorella biomass,protein and chlorophyll content were finally determined.The results showed that the model based on 1st combined with RT spectra had better predictive ability for chlorella nutrient content detection,and the root mean square errors of prediction(RMSEP)and coefficients of determination(R2)were 0.041 and 0.933 for biomass,0.012 and 0.973 for protein,and 0.517 and 0.962 for chlorophyll,respectively.This model showed practical application value,and could realize the rapid and accurate detection of chlorella biomass,protein and chlorophyll content at the same time.

[This corrects the article DOI: 10.1016/j.apsb.2022.05.019.].

Cardiac fibrosis is characterized by an elevated amount of extracellular matrix (ECM) within the heart. However, the persistence of cardiac fibrosis ultimately diminishes contractility and precipitates cardiac dysfunction. Circular RNAs (circRNAs) are emerging as important regulators of cardiac fibrosis. Here, we elucidate the functional role of a specific circular RNA CELF1 in cardiac fibrosis and delineate a novel feedback loop mechanism. Functionally, circ-CELF1 was involved in enhancing fibrosis-related markers' expression and promoting the proliferation of cardiac fibroblasts (CFs), thereby exacerbating cardiac fibrosis. Mechanistically, circ-CELF1 reduced the ubiquitination-degradation rate of BRPF3, leading to an elevation of BRPF3 protein levels. Additionally, BRPF3 acted as a modular scaffold for the recruitment of histone acetyltransferase KAT7 to facilitate the induction of H3K14 acetylation within the promoters of the Celf1 gene. Thus, the transcription of Celf1 was dramatically activated, thereby inhibiting the subsequent response of their downstream target gene Smad7 expression to promote cardiac fibrosis. Moreover, Celf1 further promoted Celf1 pre-mRNA transcription and back-splicing, thereby establishing a feedback loop for circ-CELF1 production. Consequently, a novel feedback loop involving CELF1/circ-CELF1/BRPF3/KAT7 was established, suggesting that circ-CELF1 may serve as a potential novel therapeutic target for cardiac fibrosis.